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HLTH331 > Week 4: Lipids > Flashcards

Week 4: Lipids Flashcards

1
Q

Simple lipids

A

Two types of products from hydrolysis

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2
Q

Compound/complex lipids

A

Three or more products from hydrolysis

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3
Q

Derived lipids

A

Combined simple and compound lipids through hydrolysis

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4
Q

Types of simple lipids

A

a) Waxes
b) Triglycerides

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5
Q

What are triglycerides further broken into?

A

Glycerol and fatty acids

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6
Q

What are fatty acids further broken into?

A

Saturated fatty acids
Unsaturated fatty acids

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7
Q

What are unsaturated fatty acids further broken down into?

A

Monounsaturated
Polyunsaturated

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8
Q

Monounsaturated fatty acids

A

Oleic acid (ex. olive oil)

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9
Q

Polyunsaturated fatty acids

A

Linoliec acid (omega-6)
Linolenic acid (omega-3)

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10
Q

Compound lipids

A

Phospholipid
Glycolipid (Cerbrosides and gangliosides)

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11
Q

Derived lipids

A

a) Steroids
b) Sterols
c) Carotenoids

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12
Q

Steroids

A

Bile acids, sex hormones

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13
Q

Sterols

A

Cholesterol, ergosterol

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14
Q

Carotenoids

A

Carotene, xanthophils

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15
Q

What are triglycerides composed of?

A

3 fatty acids with a glycerol

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16
Q

Types of triglycerides

A
  1. Saturated
  2. Monounsaturated
  3. Polyunsaturated
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17
Q

Saturated fatty acids and bonds

A

No double bonds, all carbons have max amount of hydrogen bonds

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18
Q

What foods contain saturated fatty acids ?

A

Animal fats and plant oils
ex. butter, meats

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19
Q

Monounsaturated fatty acids and bonds

A

One double bond

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20
Q

Polyunsaturated fatty acids and bonds

A

More than one double bond

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21
Q

Structure of sterols

A

Four-ring steroid nucleus and at least one hydroxyl group

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22
Q

Cholesterol

A

Most common sterol, 25% of plasma membrane in some nerve cells

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23
Q

How does cholesterol exist?

A

Can exist in free form or hydroxyl group at C-3 can be esterified w a fatty acid

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24
Q

How is cholesterol regulated in membranes

A

Cells esterify excess cholesterol with a fatty acid and store the cholesterol esters in vesicles with the cytosol
When free cholesterol is needed, cholesterol esters are hydrolyzed and it is transported to membrane

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25
Q

What is cholesterol a precursor for?

A

Corticosteroid hormones, sex hormones, bile salts, vitamin D3

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26
Q

Lipid digestion in the mouth

A

Lingual lipase breaks triglycerides into triacylglycerols, fatty acids and diacylglycerols

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27
Q

Lipid digestion in the stomach

A

Gastric lipase breaks them down even more

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28
Q

Where does most of lipid digestion occur?

A

Lumen of small intestine

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29
Q

Lipid digestion in the small intestine- bile

A

Bile breaks down triacylglycerols, fatty acids and diacylglycerols into emulsified triacylglycerols, fatty acids and diacylglycerol micelles via emulsification

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30
Q

Lipid digestion in small intestine- pancreatic lipase

A

Breaks down triacylglycerols, fatty acids and diacylglycerol micelles into monoacylglycerols and fatty acids by enzymatic digestion

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31
Q

What do micelles contain?

A

Contain the final digestion products from lipid hydrolysis such as free long FA, monoacylglycerols, lysophospholipids, free cholesterol, phytoesterols, fat-soluble vitamins

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32
Q

What are micelles?

A

Lipid molecules w a hydrophobic core and a hydrophilic shell that allows lipids to travel through a polar solvent
Produced in liver

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33
Q

How do micelles transport lipids into enterocytes?

A

They are water soluble and penetrate the water layer bathing the enterocytes of the small intestine, they interact w microvilli at the brush border and lipids diffuse into enterocytes

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34
Q

What are esterases?

A

Digestive enzymes that break down dietary lipids in GI tract

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35
Q

What do esterases do?

A

Cleave ester bonds with triglycerides, phospholipids and cholesterol esters

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36
Q

How are cholesterol esters absorbed?

A

Cannot be absorbed, must be hydrolyzed into free cholesterol and fatty acids to be incorporated into micelle

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37
Q

Lipid absorption

A
  1. Inside mucosal cells of small intestine, fatty acids and monoglycerides are reassembled into lipids by esterification forming chylomicrons
  2. Chylomicrons enter lymph vessel
  3. Travel to left subclavian vein and diffuses into circulation
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38
Q

What are monoacylglycerols and diacylglycerols and fatty acids reassembled into?

A

Triglycerides

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39
Q

What is cholesterol reassembled into?

A

Cholesterol ester

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40
Q

What are lysophospholipids and fatty acids reassembled into?

A

Phospholipids

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41
Q

Where do chylomicrons bipass?

A

The liver so that they aren’t catabolized

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42
Q

Lipoproteins

A

Lipids are transported in blood as components of lipoproteins

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43
Q

Types of lipoproteins

A

Chylomicrons
Very low density lipoproteins (VLDL)
Low density lipoproteins (LDL)
Intermediate-density lipoprotein (IDL)
High-density lipoprotein (HDL)

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44
Q

Lipoprotein metabolism differs depending on

A
  1. Which lipids are transported (triglycerides, cholesterol, phospholipids)
  2. Where lipids are delivered (liver, skeletal muscle, adipose tissue)
  3. Lipoprotein metabolic fate
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45
Q

Exogenous lipid transport

A

Transport of dietary lipids (triacylglycerols) from the intestine to peripheral tissues for storage and energy utilization

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46
Q

Pathway of exogenous transport

A

After chylomicrons enter the blood stream, triglycerides are transferred to skeletal muscle and adipose tissue, leading to the formation of a chylomicron remnant which results in delivery of cholesterol to liver

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47
Q

When does exogenous lipid transport occur?

A

Operates only after a fat containing meal

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48
Q

What happens to chylomicrons at the end of exogenous lipid transport?

A

Chylomicrons disappear after all dietary triacylglycerols are delivered to target tissues

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49
Q

What lipoprotein is involved in exogenous lipid transport?

A

Chylomicrons

50
Q

Endogenous lipid transport

A

Transport of triglycerides (already in body) from liver to peripheral tissue for storage or energy utilization

51
Q

What lipoproteins are involved in endogenous lipid transport?

A

VLDL, IDL, LDL

52
Q

Reverse cholesterol transport

A

Ability of HDL to pick up excess cholesterol from peripheral tissues and deliver it to liver for excretion from body by bile

53
Q

Lipoprotein involved in reverse cholesterol transport

A

HDL

54
Q

Step 1 of reverse cholesterol transport

A

Lipid free ApoA-1 is secreted by liver and intestines and released from chylomicrons and VLDL during hydrolysis

55
Q

Step 2 of reverse cholesterol transport

A

ApoA-1 acquires PL and C from interaction w liver resulting in nascent HDL particles

56
Q

Step 3 of reverse cholesterol transport

A

Nascent HDL acquires more PL and C from non-hepatic tissues

57
Q

Step 4 of reverse cholesterol transport

A

LCAT enzyme (carried on HDL) forms cholesterol esters by catalyzing the transfer of fatty acids to free cholesterols and CE migrates to core of HDL particle

58
Q

Step 5 of reverse cholesterol transport

A

Continuous binding to cell receptors and continued action of LCAT causes HDL to grow in size

59
Q

Step 6 of reverse cholesterol transport

A

Accumulated CE can be transferred to other lipoproteins through CEPT which distributes VLDL to LDL so that HDL is reduced in size to optimize interaction with receptors

60
Q

Step 7 of reverse cholesterol transport

A

HDL binds with receptors on hepatocytes and either CE is deposited in liver cells and depleted HDL returns to circulation OR entire HDL is internalized and degraded

61
Q

Why is a larger HDL beneficial?

A

Greater ability to gather cholesterol and deliver it to the liver and therefore reduced CVD risk

62
Q

Atherosclerosis

A

Progressive narrowing of the arteries caused by a buildup of plaque in the lining of the artery; major cause of CVD

63
Q

Plaque

A

Composed of fats, cholesterol etc.

64
Q

Steps of developing atherosclerosis

A
  1. Dysfunctional endothelial cells and retention of ApoB containing lipoproteins
  2. Triggers an inflammatory response
  3. Fatty streak formation
65
Q

Formation of foam cells- atherosclerosis pathogenesis

A
  1. Initiation of inflammatory response triggers monocytes and T-lymphocytes to adhere to the endothelium of arteries, changing their shape and loosening their tight junctions
  2. Allows LDL (carrying triglycerides and cholesterol) to enter arterial wall and become trapped in intima
  3. LDL is oxidized
  4. Monocytes become macrophages which accept oxidized LDL by phagocytosis, forming foam cells
66
Q

Foam cells function

A

Recruitment and proliferation of smooth muscle cells, further LDL oxidation, recruitment of other inflammatory cells and additional impairment of endothelial function
LEAD TO FATTY STREAK

67
Q

Plaque formation- atherosclerosis

A

Over time, accumulation of foam cells results in a fibrous plaque in the walls of the arteries

68
Q

LDL-C and risk of CVD

A

Causal and cumulative effect

69
Q

The lipid hypothesis

A

States that elevated plasma cholesterol (LDL cholesterol) has a causal role in the development of heart disease and CVD

70
Q

Does dietary cholesterol impact blood cholesterol?

A

Not necessarily bc 80% of cholesterol is produced in the body and only 20% comes from the food you eat

71
Q

Ratio of ApoA to ApoB and CVD risk

A

Decreasing ratio = decreased risk

72
Q

Dangerous cholesterol levels

A

Total= 240+
LDL= 60+
HDL male= under 40, female = under 50

73
Q

Healthy cholesterol levels

A

Total= under 200
LDL= under 100
HDL 60+

74
Q

What impact do saturated fats have on LDL receptors?

A

Saturated fat decreases sensitivity of LDL receptor on liver, increasing LDL cholesterol

75
Q

Does dose matter in studies that try to replace saturated fats in diet?

A

Yes
Only a certain range of %energy from saturated fat will increase risk of CVD event

76
Q

Does nutrient replacement matter when replacing saturated fats in diet?

A

Yes
No effect when replaced w carbs or MUFA
Positive effect when replaced with PUFA

77
Q

Does source matter when replacing saturated fat in diet?

A

Yes
Vegetable sources of fat and PUFA reduce risk of CVD more than dairy fat, and especially more than animal fat

78
Q

Does type of carb matter when replacing saturated fat in diet?

A

Yes
Replacing saturated fat with high quality carbs reduces risk of CVD but replacement with refined starch and added sugars doesn’t

79
Q

Three main types of omega-3 (polyunsaturated fat)

A
  1. EPA
  2. DHA
  3. ALA
80
Q

Roles of omega-3

A
  1. Components of phospholipid (increase permeability of plasma membrane)
  2. Precursor for inflammatory molecules: resolvins, protectins, maresins
  3. Cardiovascular benefits
81
Q

Sources of omega-3

A

Fish-salmon
Flax seed

82
Q

DRI of omega-3 for adults

A

Men 19+= 1.6g/day
Women 19+= 1.1 g/day

83
Q

AI for ALA for ages 0-12 months

A

0.5g/day

84
Q

AI for ALA for ages 1-3

A

0.7g/day

85
Q

AI for ALA for ages 4-8

A

0.9g/day

86
Q

AI for ALA for ages 9-13 boys

A

1.2g/day

87
Q

AI for ALA for ages 9-13 girls

A

1.0g/day

88
Q

AI for ALA for ages 14-18 boys

A

1.6g/day

89
Q

AI for ALA for ages 14-18 girls

A

1.1g/day

90
Q

Recommended intake of ALA per week

A

2 servings of oily fish per week

91
Q

History of Omega-3 literature- cross sectional studies

A

Greenland eskimos have reduced risk of CVD bc they have more EPA in diet

92
Q

History of omega-3 literature- case control studies

A

Risk of a CV event decreased the most when subjects ate btwn 2.94 and 5.54g of fish per week

93
Q

Omega-3 index

A

Level of EPA and DHA in erythrocyte (RBC) phospholipids
Used as a risk factor for CHD and death from CHD

94
Q

Levels on the omega-3 index

A

<4% high risk
4-8% moderate-high risk
>8% lowest risk

95
Q

Blood levels of DHA and EPA and risk of death from CHD

A

Low = increased risk

96
Q

Primary prevention

A

Intervening before health effects occur (usual risk population)

97
Q

Secondary prevention

A

Known CVD/CHD, previous MI, stroke etc.

98
Q

Primary outcome measures

A

Cardiovascular outcomes
Coronary outcomes
- Myocardial infarction
- Percutaneous intervention
- Sudden cardiac arrest
- coronary bypass graft
All-cause mortality
Hospitalization for CV reasons

99
Q

Composite measure

A

Usually studies measure for a variety of primary outcome measures

100
Q

Pre-2018 major trials

A

Found that omega-3 fatty acid had no effect on death from CHD

101
Q

VITAL (2019)

A

Found no sig diff btwn placebo and omega-3 group

102
Q

VITAL(2019): Subgroup analysis

A

People who ate less than 1.5 servings/week of fish saw a greater reduction in risk of MI and CV event when supplementing omega-3 than people who already ate a lot fish

103
Q

REDUCE-IT (2019)

A

Found a greater reduction in risk of a CV event in the secondary prevention cohort when supplementing w omega-3 compared to primary prevention cohort

104
Q

Post 2018 Major trials

A

Included the REDUCE-IT study
Found a stronger association that showed that omega-3 reduces risk of CV events

105
Q

Cochrane review

A

Found that increasing omega-3 reduces risk of CHD events, mostly in secondary prevention group

106
Q

Omega-3 literature limitations

A
  1. Support for omega-3 benefit comes from low quality studies
  2. Issues with control vs omega-3 pills (fishy taste)
  3. Analyses are not controlled for all variables (ex. protein consumption)
  4. Generalizability limitations (only benefit for secondary prevention populations and no standardized dose)
107
Q

Omega-3 supplementation for skeletal muscle

A

Increases EPA and DHA composition in skeletal muscle

108
Q

Fish oil supplementation and muscle protein synthesis

A

Omega-3 spikes MPS causing you to lose less muscle mass
It potentiates MPS in response to an amino acid and insulin infusion

109
Q

Omega-3 intake in older adults for skeletal muscle

A

Increases muscle mass and strength
Increased mitochondrial gene expression (easier to generate energy)

110
Q

Krill oil supplementation in older adults

A

Increased muscle function and size

111
Q

Omega-3 supplementation in older women

A

Exercise induced (RT) increases in muscle quality

112
Q

Omega-3 supplementation in older men

A

Don’t see the same benefit on muscle quality as older women

113
Q

Omega-3 fatty acid intake and muscle anabolism

A

Improves ability to gain and maintain muscle
(But this is done in older pop. who are more susceptible to muscle loss)

114
Q

Omega-3 fatty acid and muscle disuse atrophy

A

Those who take omega-3 with an immobilization injury will lose less muscle and gain more muscle back than those who don’t

115
Q

Does EPA have a benefit for health?

A

Yes, but when combined with DHA

116
Q

Fates of LDL once it enters intima of artery wall

A
  1. Moves back in to bloodstream
  2. Becomes oxidized
  3. Taken up by monocyte/macrophages which form foam cells
117
Q

Progression of atherosclerosis

A
  1. Foam cell
  2. Fatty streak
  3. Intermediate lesions
  4. Atheroma
  5. Fibrous plaque
  6. Complicated lesion/rupture
118
Q

Why are LDL third in line to be taken up by liver and non-hepatic tissue?

A

Can survive in body for 3-5 days bc LDL doesn’t supply cholesterol to organs

119
Q

What happens if LDL receptors are defective?

A

Increased plasma cholesterol which will accelerate atherosclerosis

120
Q

What can all cells do with cholesterol?

A

Synthesize cholesterol, but only liver can degrade it

HLTH331 (9 decks)

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